PMID- 22552813
OWN - NLM
STAT- MEDLINE
DCOM- 20120928
LR  - 20131121
IS  - 1791-244X (Electronic)
IS  - 1107-3756 (Linking)
VI  - 30
IP  - 1
DP  - 2012 Jul
TI  - Naringenin attenuates the release of pro-inflammatory mediators from 
      lipopolysaccharide-stimulated BV2 microglia by inactivating nuclear factor-kappaB and 
      inhibiting mitogen-activated protein kinases.
PG  - 204-10
LID - 10.3892/ijmm.2012.979 [doi]
AB  - Naringenin, one of the most abundant flavonoids in citrus fruits and grapefruits, 
      has been reported to exhibit anti-inflammatory and antitumor activities. However, 
      the cellular and molecular mechanisms underlying the naringenin anti-inflammatory 
      activity are poorly understood. In this study, we conducted an investigation of 
      the inhibitory effects of naringenin on the production of lipopolysaccharide 
      (LPS)-induced pro-inflammatory mediators in BV2 microglial cells. We found that 
      pre-treatment with naringenin prior to treatment with LPS significantly inhibited 
      excessive production of nitric oxide (NO) and prostaglandin E2 (PGE2) in a 
      dose-dependent manner. The inhibition was associated with downregulation of 
      inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. 
      Naringenin also attenuated the production of pro-inflammatory cytokines and 
      chemokines, including interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and 
      monocyte chemoattractant protein-1 (MCP-1) by suppressing expression of mRNAs for 
      these proteins. In addition, the molecular mechanism underlying 
      naringenin-mediated attenuation in BV2 cells has a close relationship to 
      suppressing translocation of the nuclear factor-kappaB (NF-kappaB) p65 subunit into the 
      nucleus and the phosphorylation of Akt and mitogen-activated protein kinases 
      (MAPKs). These findings suggest that naringenin may provide neuroprotection 
      through suppression of pro-inflammatory pathways in activated BV2 microglial 
      cells.
FAU - Park, Hye Young
AU  - Park HY
AD  - Department of Biochemistry, Dongeui University College of Oriental Medicine, 
      Busan 614-052, Republic of Korea.
FAU - Kim, Gi-Young
AU  - Kim GY
FAU - Choi, Yung Hyun
AU  - Choi YH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120423
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Flavanones)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (RNA, Messenger)
RN  - 0 (Rela protein, mouse)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - HN5425SBF2 (naringenin)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents, Non-Steroidal/*pharmacology
MH  - Chemokine CCL2/biosynthesis/genetics
MH  - Cyclooxygenase 2/biosynthesis
MH  - Dinoprostone/biosynthesis
MH  - Flavanones/*pharmacology
MH  - Inflammation/genetics/immunology/metabolism
MH  - Inflammation Mediators/immunology/*metabolism
MH  - Interleukin-1beta/biosynthesis/genetics
MH  - Lipopolysaccharides
MH  - Mice
MH  - Microglia/*metabolism
MH  - Mitogen-Activated Protein Kinases/*antagonists & inhibitors/metabolism
MH  - NF-kappa B/*antagonists & inhibitors/metabolism
MH  - Neuroprotective Agents/pharmacology
MH  - Nitric Oxide/biosynthesis
MH  - Nitric Oxide Synthase Type II/biosynthesis
MH  - Phosphorylation
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - RNA, Messenger/biosynthesis
MH  - Transcription Factor RelA/metabolism
MH  - Tumor Necrosis Factor-alpha/biosynthesis/genetics
EDAT- 2012/05/04 06:00
MHDA- 2012/09/29 06:00
CRDT- 2012/05/04 06:00
PHST- 2012/01/25 00:00 [received]
PHST- 2012/03/23 00:00 [accepted]
PHST- 2012/05/04 06:00 [entrez]
PHST- 2012/05/04 06:00 [pubmed]
PHST- 2012/09/29 06:00 [medline]
AID - 10.3892/ijmm.2012.979 [doi]
PST - ppublish
SO  - Int J Mol Med. 2012 Jul;30(1):204-10. doi: 10.3892/ijmm.2012.979. Epub 2012 Apr 
      23.